Evidence map›Paper›PMID 39242435›Full record

ArticleLung2024

Utility of the 52-Gene Risk Score to Identify Patients with Idiopathic Pulmonary Fibrosis at Greater Risk of Mortality in the Era of Antifibrotic Therapy.

Julia F Söllner, Stefan Bentink, Christian Hesslinger, Thomas B Leonard, Megan L Neely, Nina M Patel, Thomas Schlange, Jamie L Todd, Richard Vinisko, Margaret L Salisbury and 1 more

Abstract read
In one paragraph

Article in Lung, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Article
  2. Progressive pulmonary fibrosis: the importance of identification and intervention.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  3. Article
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Julia F SöllnerBoehringer Ingelheim Pharma GmbH and Co. KG, Biberach, Germany. julia.soellner@boehringer-ingelheim.com.
Stefan BentinkStaburo GmbH, Munich, Germany.
Christian HesslingerBoehringer Ingelheim Pharma GmbH and Co. KG, Biberach, Germany.
Thomas B LeonardBoehringer Ingelheim Pharmaceuticals, Inc., Ridgefield, CT, USA.
Megan L NeelyDuke Clinical Research Institute, Durham, NC, USA.ORCID 0000-0002-0101-1081
Nina M PatelBoehringer Ingelheim Pharmaceuticals, Inc., Ridgefield, CT, USA.
Thomas SchlangeBoehringer Ingelheim Pharma GmbH and Co. KG, Biberach, Germany.ORCID 0000-0002-2027-3976
Jamie L ToddDuke Clinical Research Institute, Durham, NC, USA.ORCID 0000-0003-4247-3693
Richard ViniskoBoehringer Ingelheim Pharmaceuticals, Inc., Ridgefield, CT, USA.
Margaret L SalisburyVanderbilt University Medical Center, Nashville, TN, USA.ORCID 0000-0001-8217-6955
IPF-PRO Registry investigators

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeWe investigated whether a 52-gene signature was associated with transplant-free survival and other clinically meaningful outcomes in patients with idiopathic pulmonary fibrosis (IPF) in the IPF-PRO Registry, which enrolled patients who were and were not taking antifibrotic therapy.

methodsThe 52-gene risk signature was implemented to classify patients as being at "high risk" or "low risk" of disease progression and mortality. Transplant-free survival and other outcomes were compared between patients with a low-risk versus high-risk signature.

resultsThe 52-gene signature classified 159 patients as at low risk and 86 as at high risk; in these groups, respectively, 56.6% and 51.2% used antifibrotic therapy at enrollment. Among those taking antifibrotic therapy, patients with a low-risk versus high-risk signature were at decreased risk of death, a composite of lung transplant or death, and a composite of decline in DLco % predicted > 15%, lung transplant, or death. Similar results were observed in the overall cohort.

conclusionsThese data suggest that the 52-gene signature can be used in patients with IPF treated with antifibrotic therapy to distinguish patients at higher risk of disease progression and mortality.

Indexed as

Antifibrotic AgentsDisease ProgressionIdiopathic Pulmonary FibrosisLung TransplantationRegistriesAgedFemaleGene Expression ProfilingHumansMaleMiddle AgedPulmonary Diffusing CapacityRisk AssessmentRisk FactorsAntifibrotic AgentsGene expression profilingInterstitial lung diseasesObservational studyPrognosis

Identifiers

PMID39242435
PMCPMC11427488

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.